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VX (nerve agent)
Identifiers
CAS number 50782-69-9 Yes check.svgY
SMILES
Properties
Molecular formula C11H26NO2PS
Density 1.00083 g/mL
Melting point

-50 °C, 223 K, -58 °F

Boiling point

298 °C, 571 K, 568 °F

Vapor pressure 0.0007 mmHg (0.09 Pa) at 25 °C
Hazards
NFPA 704
NFPA 704.svg
1
4
1
Flash point 159 °C[1]
 Yes check.svgY (what is this?)  (verify)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

VX, IUPAC name O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothioate, is an extremely toxic substance whose only application is in chemical warfare as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations in UN Resolution 687. The production and stockpiling of VX was outlawed by the Chemical Weapons Convention of 1993.

The VX nerve agent is the most well-known of the V-series of nerve agents and is considered an area denial weapon due to its physical properties.

Contents

Discovery

Dr. Ranajit Ghosh, a chemist at the Plant Protection Laboratories of Imperial Chemical Industries was investigating a class of organophosphate compounds (organophosphate esters of substituted aminoethanethiols). Like Gerhard Schrader, an earlier investigator of organophosphates, Dr. Ghosh found that they were quite effective pesticides. In 1954, ICI put one of them on the market under the trade name Amiton. It was subsequently withdrawn, as it was too toxic for safe use. The toxicity did not go unnoticed, and samples of it had been sent to the British Armed Forces research facility at Porton Down for evaluation. After the evaluation was complete, several members of this class of compounds would become a new group of nerve agents, the V agents. The best known of these is probably VX, assigned the UK Rainbow Code Purple Possum, with the Russian V-Agent coming a close second (Amiton is largely forgotten as VG). This class of compounds is also sometimes known as Tammelin's esters, after Lars-Erik Tammelin of the Swedish Institute of Defense Research. Dr. Tammelin was also conducting research on this class of compounds in 1952, but for obvious reasons he did not publicize his work widely.

Chemical characteristics

With its high viscosity and low volatility, VX has the texture and feel of motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odorless and tasteless, and can be distributed as a liquid, both pure and as a mixture with a polymer in the form of thickened agent, or as an aerosol. It works as a nerve agent by blocking the function of the enzyme acetylcholinesterase. Normally, an electric nerve pulse would cause the release of acetylcholine over a synapse that would stimulate muscle contraction. The acetylcholine is then broken down to non-reactive substances (acetic acid and choline) by the acetylcholinesterase enzyme. If more muscle tension is needed the nerve must release more acetylcholine. VX blocks the action of acetylcholinesterase, thus resulting in initial violent contractions, followed by sustained supercontraction restricted to the subjunctional endplate sarcoplasm and prolonged depolarizing neuromuscular blockade, the latter resulting in flaccid paralysis of all the muscles in the body. Sustained paralysis of the diaphragm muscle causes death by asphyxiation.

Synthesis

VX is produced via the "transester process". This entails a series of steps whereby phosphorus trichloride is methylated to produce methyl phosphonous dichloride. The resulting material is reacted with ethanol to form a diester. This is then transesterified with N',N'-diisopropylaminoethanol to produce the mixed phosphonite. Finally, this immediate precursor is reacted with sulfur to form VX.

VX TransesterProcess.png

VX can also be delivered in binary chemical weapons which mix in-flight to form the agent prior to release. Binary VX is referred to as VX2,[2] and is created by mixing aO-(2-diisopropylaminoethyl) O'-ethyl methylphosphonite (Agent QL) with elemental sulfur (Agent NE) as is done in the Bigeye aerial chemical bomb. It may also be produced by mixing with sulfur compounds, as with the liquid dimethyl polysulfide mixture (Agent NM) in the canceled XM-768 8-inch binary projectile program.[citation needed]

Solvolysis

Like other organophosphorus nerve agents, VX may be destroyed by reaction with strong nucleophiles such as pralidoxime. The reaction of VX with concentrated aqueous sodium hydroxide results in competing cleavage of the P-O and P-S esters, with P-S cleavage dominating. This is somewhat problematic, since the product of P-O bond cleavage (named EA 2192) remains toxic. In contrast, reaction with the anion of hydrogen peroxide (hydroperoxidolysis) leads to exclusive cleavage of the P-S bond.[3],[4]

VX-solvolysis-P-S-2D-skeletal.png P-S cleavage
NaOH(aq) reacts with VX in two ways. It can cleave VX's P-S bond, yielding two relatively nontoxic products...
VX-solvolysis-P-O-2D-skeletal.png P-O cleavage
...or it can cleave VX's P-O bond, forming ethanol and EA 2192 (shown in red), which has similar toxicity to VX itself

Biological effects

VX is the most toxic nerve agent ever synthesized for which activity has been independently confirmed.[5] The median lethal dose (LD50) for humans is estimated to be about 10 milligrams through skin contact and the LCt50 for inhalation is estimated to be 30–50 mg·min/m³.[6]

Early symptoms of percutaneous exposure (skin contact) may be local muscular twitching or sweating at the area of exposure followed by nausea or vomiting. Some of the early symptoms of a VX vapor exposure to nerve agent may be rhinorrhea (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). Miosis (pinpointing of the pupils) may be an early sign of agent exposure but is not usually used as the only indicator of exposure.[7]

Treatment

Primary consideration should be given to removal of the liquid agent from the skin before removal of the individual to an uncontaminated area or atmosphere. After removal from the contaminated area, the casualty will be decontaminated by washing the contaminated areas with household bleach and flushing with clean water. After decontamination, the contaminated clothing is removed and skin contamination washed away. If possible, decontamination is completed before the casualty is taken for further medical treatment.

An individual who has received a known nerve-agent exposure or who exhibits definite signs or symptoms of nerve-agent exposure should immediately have the nerve agent antidote drugs atropine, pralidoxime (2-PAM), and diazepam injected. In several nations the nerve agent antidotes are issued for military personnel in the form of an autoinjector such as the United States military Mark I NAAK.[7]

Atropine works by binding and blocking a subset of acetylcholine receptors (known as muscarinic acetylcholine receptor, mAchR), so that the build up of acetylcholine produced by loss of the acetylcholinesterase function can no longer affect their target. The injection of pralidoxime regenerates bound acetylcholinesterase.

Diagnostic tests

Controlled studies in humans have shown that minimally toxic doses cause 70-75% depression of erythrocyte cholinesterase within several hours of exposure. The serum level of ethyl methylphosphonic acid (EMPA), a VX hydrolysis product, was measured to confirm exposure in one poisoning victim.[8]

History

For an in-depth discussion, see main article on nerve agent history

The chemists Ranajit Ghosh and J.F. Newman discovered the V-series nerve agents at ICI in 1952, patenting diethyl S-2-diethylaminoethyl phosphono- thioate (agent VG) in November, 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered. Information on the substance was passed to Porton Down in 1954 and research there led to VX within a year. This was traded to the United States as the British passed over VX in favor of continuing with sarin as the UK chemical weapon of choice, the reasoning behind the decision is unclear, although the then recent completion of a sarin production facility at Nancekuke may have played a part.

The US then went into production of large amounts of VX in 1961 at Newport Chemical Depot.

Iraq under Saddam Hussein admitted to UNSCOM that it had researched VX, but had failed to weaponize the agent due to production failure. After U.S. and allied forces had invaded Iraq, no proof of weaponized VX was found.[1] Subsequent investigation after the 2003 Invasion of Iraq indicates that Iraq had indeed weaponized VX in 1988, and had dropped three VX-filled bombs on Iran.[2]

In December 1994 and January 1995, Masami Tsuchiya of AUM Shinrikyo synthesized 100 to 200 grams of VX which was used to attack three persons. Two persons were injured and one 28-year-old man died, who is believed to be the only victim of VX ever documented in the world.[9] The VX victim, whom Shoko Asahara had suspected as a spy, was attacked at 7:00 am on December 12, 1994 on the street in Osaka by Tomomitsu Niimi and another AUM member, who sprinkled the nerve agent on his neck. He chased them for about 100 yards (100 m) before collapsing, dying 10 days later without ever coming out of a deep coma. Doctors in the hospital suspected at the time he had been poisoned with an organophosphate pesticide. But the cause of death was pinned down only after cult members arrested for the subway attack confessed to the killing. Ethyl methylphosphonate, methylphosphonic acid and diisopropyl-2-(methylthio) ethylamine were later found in the body of the victim. Unlike the cases for sarin (Matsumoto incident and Sarin gas attack on the Tokyo subway), VX was not used for mass murder.

The only countries known to possess VX are the United States and Russia.[5] A Sudanese pharmaceutical facility was bombed by the U.S. in 1998 acting on information that it used VX and that the origin of the agent was associated with both Iraq and Al Qaeda.[3][10] The chemical in question was later identified as O-ethyl hydrogen methylphosphonothioate (EMPTA), used as a precursor in the production of VX. It is also used to treat seeds and turf grasses.[11]

US VX stockpile elimination

In the late 1960s, the US canceled its chemical weapons programs and began the destruction of its stockpiles of agents by a variety of methods. Early disposal included the US Army's CHASE (Cut Holes And Sink 'Em) program, in which old ships were filled with chemical weapons stockpiles and then scuttled. CHASE 8[citation needed] was conducted on June 15, 1967, in which the S.S. Cpl. Eric G. Gibson was filled with 7,380 VX rockets and scuttled in 7,200 feet (2,200 m) of water, off the coast of Atlantic City, New Jersey.

As of FY2008 the US Department of Defense reported that it dumped at least 124 tons of VX into the Atlantic Ocean off the coasts of New York/New Jersey and Florida. This material consisted of nearly 22,000 M55 rockets, 19 bulk containers holding 1,400 pounds (640 kg) each, and one M23 chemical landmine.[12]

Incineration was used for VX stockpile destruction starting in 1990 with Johnston Atoll Chemical Agent Disposal System in the North Pacific with other incineration plants following at Deseret Chemical Depot, Pine Bluff Arsenal, Umatilla Chemical Depot and Anniston Army Depot with the last of the VX inventory destroyed on December 24, 2008.[13]

  • Newport Chemical Depot completed their VX stockpile destruction in August, 2008.[14]
    • Newport began VX stockpile elimination using chemical neutralization in 2005. VX is hydrolyzed to much less toxic byproducts by using concentrated caustic solution, and the resulting waste is then shipped off-site for further processing. Technical and political issues regarding this secondary byproduct resulted in some delays but most of Newport's stockpile was eliminated in 2007.

Worldwide VX stockpile elimination

Worldwide, VX disposal continues, since 1997 under the mandate of the Chemical Weapons Convention. The US is providing support for Russian destruction activities, with a program called the Nunn-Lugar program.[15] The Nunn-Lugar program has been able to convert a former Chemical Weapons Depot at Shchuchye into a facility to destroy chemical weapons. The new facility opened in May 2009, will work on eliminating the nearly 5,950 tons of nerve agents held at the former storage complex. However, this facility only holds about 14% of Russian chemical weapons that are stored throughout seven sites.[16] A new destruction plant, being built for an amount of 140 million and paid for by Germany, is to open at Potshep, region Brjansk, in 2009.

See also

References

  1. ^ "MSDS: Nerve Agent (VX)". Edgewood Chemical Biological Center (ECBC), Department of the Army. 22 December 2000. http://www.ilpi.com/msds/vx.html. Retrieved 2007-10-25. 
  2. ^ Ellison, D. Hank. Handbook of Chemical and Biological Agents, (Google Books), CRC Press, New York: 2007, p. 47, (ISBN 0849314348).
  3. ^ Yang, Yu-Chu (1999). "Chemical Detoxification of Nerve Agent VX". Acc. Chem. Res.. p. 109–115.. 
  4. ^ Daniel, Kelly et al. (2008). "Computational studies on the solvolysis of the chemical warfare agent VX". J. Phys. Org. Chem.. p. 321–328.. 
  5. ^ a b "VX". Council on Foreign Relations. 2006-01. http://www.cfr.org/publication/9556/. Retrieved 2007-03-27. 
  6. ^ Federation of American Scientists :: Types of Chemical Weapons
  7. ^ a b "US Army Toxic Chemical Agent Safety Standards" (PDF). DA PAM 385-61. Section 7-8 Self/Buddy Aid Procedures. US Army. http://www.army.mil/usapa/epubs/pdf/p385_61.pdf. Retrieved 2007-12-15. 
  8. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 1651-1652.
  9. ^ Pamela Zurer, "Japanese cult used VX to slay member" Chemical and Engineering News 1998, Vol 76 (no. 35).
  10. ^ Chomsky, Noam (October 2001). 9-11. Open Media. 
  11. ^ Coleman, Kim (2005). History of Chemical Warfare. Palmgrave MacMillan. 
  12. ^ https://www.denix.osd.mil/portal/page/portal/denix/environment/ARC/FY2008DEP/29_FY08DEPARC_App_Q_Sea_Disposal_final.pdf. Retrieved 2009-09-07
  13. ^ http://www.cma.army.mil/endofvx.aspx
  14. ^ http://www.cma.army.mil/fndocumentviewer.aspx?docid=003678571
  15. ^ http://lugar.senate.gov/nunnlugar/index.cfm
  16. ^ http://www.nytimes.com/2009/05/27/world/europe/27russia.html?ref=world

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